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Updated: Aug 5, 2026
A Rat Model of Tibial Cortex Transverse Transport for the Treatment of Lower Limb Ischemia
Published on: March 6, 2026
Tibial cortex transverse transport accelerates diabetic wound healing via systemic mobilization of non-classical
Yongkang Yang1,2, Zhaowei Jiang3, Kan Ouyang1
1Department of Sport Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, China.
Aims:
To clarify the immunomodulatory mechanisms by which tibial cortex transverse transport (TTT) accelerates wound healing in a type 2 diabetic rat model, with particular focus on the dynamics of subsets of monocytes and macrophages.
Methods:
A total of 186 male Sprague-Dawley rats were induced as diabetic via a high-fat diet and streptozotocin. A full-thickness skin defect was created on the dorsum of the foot immediately following standard TTT surgery. Wound closure was monitored photographically. At defined timepoints (days 3 to 21), wound tissues underwent histological and immunofluorescence staining (haematoxylin and eosin, Masson's trichrome, picrosirius red, CD68/iNOS/mannose) to assess re-epithelialization, collagen organization, and M1/M2 macrophage populations. Flow cytometry of bone marrow and peripheral blood (CD43 and CD172a markers) quantified classical and non-classical monocyte subsets. Monocyte/macrophage involvement was probed by depleting these cells with clodronate liposomes versus phosphate-buffered saline liposomes.
Results:
TTT-treated rats achieved complete wound closure by day 21, markedly faster than fixator or sham controls. Histology revealed enhanced re-epithelialization, a thicker epidermis, well-organized type III collagen, and normalized collagen fibre directionality. Immunofluorescence demonstrated a rapid decline in proinflammatory M1 and an increase in reparative M2 macrophages from day 5 onward. Flow cytometry showed a pronounced surge of non-classical monocytes in bone marrow on day 3, followed by elevated circulating levels on days 3 to 6. Monocyte/macrophage depletion markedly delayed healing and disrupted collagen deposition.
Conclusion:
TTT is associated with accelerated diabetic wound repair, accompanied by preferential mobilization of non-classical monocytes and increased M2 macrophage polarization at the wound site. These findings are consistent with a mechanically induced immunomodulatory process that may contribute to improved healing outcomes.
